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Biomedical subjects

J T Dowling

Publications and source records attributed to J T Dowling.

29 records · Page 2Linked to original sources
PubMed1968

Estimation of thyroxine distribution in man.

A group of 13 normal subjects were evaluated for their extrathyroidal thyroxine distribution. The method employed the measurement of the acute plasma disappearance of a thyroxine-(131)I tracer and its concomitant uptake into the liver and forearm. The analysis of these parameters allowed the theoretical construction of a four compartmental mathematical model system comprised of the plasma, extracellular fluid, hepatic, and extrahepatic thyroxine pools. The results of this analysis revealed that the exchange of thyroxine from the plasma into the hepatic and extrahepatic cellular fluid spaces appeared, in general, to be rapid, while the uptake into the extrahepatic tissues was relatively slow. The calculated distribution of thyroxine at equilibrium was estimated to be 14% in liver, 34% in extrahepatic tissues, and 26% each in the plasma and extracellular fluid pools in this group of normal subjects.

Journal Article↗
PubMed1968

Studies of peripheral thyroxine distribution in thyrotoxicosis and hypothyroidism.

Compartmental analysis of the peripheral distribution of labeled thyroxine was applied to various groups of subjects with thyrotoxicosis and hypothyroidism. It was observed that the hepatic incorporation of thyroxine was augmented in subjects with Graves' disease when compared to non-Graves' disease control groups at all levels of thyroid function. Decreased values of hepatic incorporation occurred in primary hypothyroid subjects. These lowered values were not acutely corrected by elevation of the serum thyroxine level, but were observed to be rectified after several months' therapy with exogenous thyroid hormone. These alterations of the hepatic thyroxine-(131)I incorporation were independently verified by direct quantitative liver scintiscan determinations. Employing a dual thyroxine tracer system, we were able to demonstrate that during the early phases of equilibration of a tracer dose of thyroxine, alterations in the rate of deiodination were observed to be present in the various thyroid disease states. Increased deiodination rates were found in subjects with Graves' disease and the reverse was noted in patients with primary hypothyroidism. Kinetic analysis of thyroxine compartmental distribution during this early phase of equilibration of a labeled thyroxine tracer indicated that the primary tissue uptake occurred in the liver. These findings supported the contention that the amount of labeled thyroxine incorporated in the liver may be directly related to the deiodination rate of thyroxine by that organ. The pathogenetic basis of these alterations is presently unknown.

Adolescent↗